CsrA and TnaB Coregulate Tryptophanase Activity To Promote Exotoxin-Induced Killing of Caenorhabditis elegansby Enteropathogenic Escherichia coli

Bhatt, Shantanu; Anyanful, Akwasi; Kalman, Daniel

doi:10.1128/jb.05197-11

Cited by 21 publications

(23 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Like P. aeruginosa, EPEC has been shown to both infect and kill C. elegans via a "slow killing" mechanism resulting from bacterial accumulation in the nematode intestine, as well as to form microcolonies similar to those formed during EPEC infection of cultured epithelial cells (Mellies et al 2006). On the other hand, EPEC has also been reported to cause paralysis and death of C. elegans via a "fast killing" mechanism involving secretion of diffusible exotoxins (Anyanful et al 2005;Bhatt et al 2011). The usefulness of the nematode as a simple animal model for the study of EPEC pathogenesis is validated by the fact that mutation-based analysis of specific genes required for full virulence of EPEC in mammalian systems are similarly required for maximum pathogenicity in the nematode.…”

Section: In Vivo Infection Modelsmentioning

confidence: 99%

In Vitro and In Vivo Model Systems for Studying Enteropathogenic Escherichia coli Infections

Law

Gur-Arie

Rosenshine

et al. 2013

Cold Spring Harbor Perspectives in Medicine

View full text Add to dashboard Cite

Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) belong to a group of bacteria known as attaching and effacing (A/E) pathogens that cause disease by adhering to the lumenal surfaces of their host's intestinal epithelium. EPEC and EHEC are major causes of infectious diarrhea that result in significant childhood morbidity and mortality worldwide. Recent advances in in vitro and in vivo modeling of these pathogens have contributed to our knowledge of how EPEC and EHEC attach to host cells and subvert hostcell signaling pathways to promote infection and cause disease. A more detailed understanding of how these pathogenic microbes infect their hosts and how the host responds to infection could ultimately lead to new therapeutic strategies to help control these significant enteric pathogens.

show abstract

Section: In Vivo Infection Modelsmentioning

confidence: 99%

In Vitro and In Vivo Model Systems for Studying Enteropathogenic Escherichia coli Infections

Law

Gur-Arie

Rosenshine

et al. 2013

Cold Spring Harbor Perspectives in Medicine

View full text Add to dashboard Cite

show abstract

“…A strong correlation has been demonstrated between nematode-pathogenic extraintestinal E. coli strains and strains that are capable of killing mice (29). Furthermore, enteroaggregative E. coli (EAEC), enteropathogenic E. coli (EPEC), adherent-invasive E. coli (AIEC), and uropathogenic E. coli (UPEC) have also been shown to be pathogenic to C. elegans (29,(31)(32)(33). Pathogenic bacteria cause disease in C. elegans directly through infection or indirectly by production of toxins (34).…”

mentioning

confidence: 99%

Evaluating the Pathogenic Potential of Environmental Escherichia coli by Using the Caenorhabditis elegans Infection Model

Merkx-Jacques

Coors

Brousseau

et al. 2013

Appl Environ Microbiol

View full text Add to dashboard Cite

The detection and abundance of Escherichia coli in water is used to monitor and mandate the quality of drinking and recreational water. Distinguishing commensal waterborne E. coli isolates from those that cause diarrhea or extraintestinal disease in humans is important for quantifying human health risk. A DNA microarray was used to evaluate the distribution of virulence genes in 148 E. coli environmental isolates from a watershed in eastern Ontario, Canada, and in eight clinical isolates. Their pathogenic potential was evaluated with Caenorhabditis elegans, and the concordance between the bioassay result and the pathotype deduced by genotyping was explored. Isolates identified as potentially pathogenic on the basis of their complement of virulence genes were significantly more likely to be pathogenic to C. elegans than those determined to be potentially nonpathogenic. A number of isolates that were identified as nonpathogenic on the basis of genotyping were pathogenic in the infection assay, suggesting that genotyping did not capture all potentially pathogenic types. The detection of the adhesin-encoding genes sfaD, focA, and focG, which encode adhesins; of iroN 2 , which encodes a siderophore receptor; of pic, which encodes an autotransporter protein; and of b1432, which encodes a putative transposase, was significantly associated with pathogenicity in the infection assay. Overall, E. coli isolates predicted to be pathogenic on the basis of genotyping were indeed so in the C. elegans infection assay. Furthermore, the detection of C. elegans-infective environmental isolates predicted to be nonpathogenic on the basis of genotyping suggests that there are hitherto-unrecognized virulence factors or combinations thereof that are important in the establishment of infection.

show abstract

“…While the biological relevance of this kind of "seesaw" regulation needs to be established (3), its features hint that CsrA activity may be governed according to the particular niche environment within the host and in turn coordinates the workings of the T3SS and other processes. Interestingly, CsrA also activates expression of tryptophanase in EPEC, which produces indole and derivatives of indole that can be can be toxic to Caenorhabditis elegans (321) or can affect LEE expression and attenuate disease in a mouse model of infection (322).…”

mentioning

confidence: 99%

Regulation of Bacterial Virulence by Csr (Rsm) Systems

Vakulskas

Potts

Babitzke

et al. 2015

Microbiol Mol Biol Rev

296

400

View full text Add to dashboard Cite

SUMMARY Most bacterial pathogens have the remarkable ability to flourish in the external environment and in specialized host niches. This ability requires their metabolism, physiology, and virulence factors to be responsive to changes in their surroundings. It is no surprise that the underlying genetic circuitry that supports this adaptability is multilayered and exceedingly complex. Studies over the past 2 decades have established that the CsrA/RsmA proteins, global regulators of posttranscriptional gene expression, play important roles in the expression of virulence factors of numerous proteobacterial pathogens. To accomplish these tasks, CsrA binds to the 5′ untranslated and/or early coding regions of mRNAs and alters translation, mRNA turnover, and/or transcript elongation. CsrA activity is regulated by noncoding small RNAs (sRNAs) that contain multiple CsrA binding sites, which permit them to sequester multiple CsrA homodimers away from mRNA targets. Environmental cues sensed by two-component signal transduction systems and other regulatory factors govern the expression of the CsrA-binding sRNAs and, ultimately, the effects of CsrA on secretion systems, surface molecules and biofilm formation, quorum sensing, motility, pigmentation, siderophore production, and phagocytic avoidance. This review presents the workings of the Csr system, the paradigm shift that it generated for understanding posttranscriptional regulation, and its roles in virulence networks of animal and plant pathogens.

show abstract

CsrA and TnaB Coregulate Tryptophanase Activity To Promote Exotoxin-Induced Killing of Caenorhabditis elegansby Enteropathogenic Escherichia coli

Cited by 21 publications

References 94 publications

In Vitro and In Vivo Model Systems for Studying Enteropathogenic Escherichia coli Infections

In Vitro and In Vivo Model Systems for Studying Enteropathogenic Escherichia coli Infections

Evaluating the Pathogenic Potential of Environmental Escherichia coli by Using the Caenorhabditis elegans Infection Model

Regulation of Bacterial Virulence by Csr (Rsm) Systems

Contact Info

Product

Resources

About